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Updated: Aug 26, 2025

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
09:01

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies

Published on: July 3, 2025

224

Modeling YAP fusions: a paradigm for investigating rare cancers?

Solmaz Sahebjam1, Mark R Gilbert1

  • 1Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA.

Genes & Development
|October 7, 2022
PubMed

Insights

Loss of the NF2 gene or YAP1 fusions promote meningioma growth by activating YAP1-TEAD. Inhibiting this interaction may offer a new therapeutic strategy for meningiomas.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Loss of the NF2 tumor suppressor gene is common in meningiomas.
  • YAP1 fusions are found in pediatric NF2 wild-type meningiomas.

Purpose of the Study:

  • To investigate the role of TEAD-dependent YAP1 activity in meningioma tumorigenesis.
  • To explore the therapeutic potential of inhibiting YAP1-TEAD interactions.

Main Methods:

  • Analysis of NF2 gene status and YAP1 fusions in meningiomas.
  • Assessment of TEAD-dependent YAP1 activity in tumor development.
  • Pharmacological inhibition of YAP1-TEAD interaction.

Main Results:

  • TEAD-dependent YAP1 activity, driven by NF2 loss or YAP1-MAML2 fusion, promotes meningioma growth.
  • Pharmacological inhibition of YAP1-TEAD showed antitumor effects in both NF2 mutant and YAP1 fusion-positive meningiomas.

Conclusions:

  • Disruption of the YAP1-TEAD interaction is a potential therapeutic strategy for meningiomas.
  • Targeting YAP1-TEAD warrants further investigation for meningioma treatment.
Keywords:
HippoNF2YAP1YAP1-MAML2gene fusionmeningioma

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